Separation of factors responsible for change in breathing pattern induced by instrumentation

1985 ◽  
Vol 59 (5) ◽  
pp. 1515-1520 ◽  
Author(s):  
W. Perez ◽  
M. J. Tobin

Employment of mouthpiece and noseclips (MP + NC) has repeatedly been shown to increase tidal volume (VT), but its effect on respiratory frequency (f) and its subsets is controversial. The mechanisms accounting for this alteration in breathing pattern are poorly understood and may include stimulation of oral or nasal sensory receptors or alteration in the route of breathing. In this study we demonstrated that use of a MP + NC, compared with nonobtrusive measurement with a calibrated respiratory inductive plethysmograph, alters the majority of the volume and time indexes of breathing pattern, with increases in minute ventilation (P less than 0.01), VT (P less than 0.001), inspiratory time (TI, P less than 0.05), expiratory time (TE, P less than 0.05), mean inspiratory flow (P less than 0.05), and mean expiratory flow (P less than 0.05) and a decrease in f(P less than 0.05). Separating the potential mechanisms we found that when the respiratory route was not altered, independent oral stimulation (using an occluded MP) or nasal stimulation (by applying paper clips to the alae nasi) did not change the breathing pattern. In contrast, obligatory oral breathing without additional stimulation of the oral or nasal sensory receptors caused increases in VT (P less than 0.05), TI (P less than 0.05), and TE (P less than 0.01) and a fall in f(P less than 0.05). Heating and humidifying the inspired air did not prevent the alteration in breathing pattern with a MP. Thus change in the respiratory route is the major determinant of the alteration in breathing pattern with a MP + NC.

1994 ◽  
Vol 76 (3) ◽  
pp. 1330-1339 ◽  
Author(s):  
H. V. Forster ◽  
T. F. Lowry ◽  
L. G. Pan ◽  
B. K. Erickson ◽  
M. J. Korducki ◽  
...  

We determined the effect of pulmonary vagal (hilar nerve) denervation (HND) and diaphragm deafferentation (DD) on inspiratory load compensation. We studied awake intact (I; n = 10), DD (n = 5), HND (n = 4), and DD+HND (n = 7) ponies at rest and during mild (1.8 mph, 5% grade) and moderate (1.8 mph, 15% grade) treadmill exercise before, during, and after resistance of the inspiratory circuit was increased from approximately 1.5 to approximately 20 cmH2O.l–1.s. During the first loaded breath in I ponies at rest, inspiratory time (TI) increased, expiratory time decreased, and inspiratory drive increased. There were minimal changes after the first breath, and inspiratory minute ventilation (VI) and arterial PCO2 did not change (P > 0.10) from control values. On the first loaded breath during exercise, TI increased but inspiratory drive either did not change or decreased from control values. TI and drive increased after the first breath, but the increases were insufficient to maintain VI and arterial PCO2 at control levels. First-breath load compensation remained after DD, HND, and DD+HND, but after DD+HND tidal volume and VI were compensated 5–10% less (P < 0.05) than in I ponies. In all groups inspiratory drive, tidal volume, and VI were markedly augmented on the first breath after loading was terminated with a gradual return toward control. We conclude that diaphragm and pulmonary afferents contribute to but are not essential for inspiratory load compensation in awake ponies.


2000 ◽  
Vol 88 (5) ◽  
pp. 1907-1914 ◽  
Author(s):  
Dean M. Robinson ◽  
Henry Kwok ◽  
Brandon M. Adams ◽  
Karen C. Peebles ◽  
Gregory D. Funk

We examined developmental changes in breathing pattern and the ventilatory response to hypoxia (7.4% O2) in unanesthetized Swiss CD-1 mice ranging in age from postnatal day 0 to 42(P0–P42) using head-out plethysmography. The breathing pattern of P0 mice was unstable. Apneas were frequent at P0 (occupying 29 ± 6% of total time) but rare by P3 (5 ± 2% of total time). Tidal volume increased in proportion to body mass (∼10–13 ml/kg), but increases in respiratory frequency (f) (55 ± 7, 130 ± 13, and 207 ± 20 cycles/min for P0, P3, and P42, respectively) were responsible for developmental increases in minute ventilation (690 ± 90, 1,530 ± 250, and 2,170 ± 430 ml ⋅ min− 1 ⋅ kg− 1for P0, P3, and P42, respectively). Between P0 and P3, increases in f were mediated by reductions in apnea and inspiratory and expiratory times; beyond P3, increases were due to reductions in expiratory time. Mice of all ages showed a biphasic hypoxic ventilatory response, which differed in two respects from the response typical of most mammals. First, the initial hyperpnea, which was greatest in mature animals, decreased developmentally from a maximum, relative to control, of 2.58 ± 0.29 in P0 mice to 1.32 ± 0.09 in P42mice. Second, whereas ventilation typically falls to or below control in most neonatal mammals, ventilation remained elevated relative to control throughout the hypoxic exposure in P0 (1.73 ± 0.31), P3 (1.64 ± 0.29), and P9 (1.34 ± 0.17) mice but not in P19 or P42 mice.


1985 ◽  
Vol 59 (4) ◽  
pp. 1090-1097 ◽  
Author(s):  
P. A. Easton ◽  
C. Jadue ◽  
M. E. Arnup ◽  
R. C. Meatherall ◽  
N. R. Anthonisen

To evaluate the contribution of vagal airway receptors to ventilatory control during hypercapnia, we studied 11 normal humans. Airway receptor block was induced by inhaling an aerosol of lidocaine; a preferential upper oropharyngeal block was also induced in a subgroup by gargling a solution of the anesthetic. Inhalation of lidocaine aerosol adequate to increase cough threshold, as measured by citric acid, did not change the ventilatory response to CO2, ratio of the change in minute ventilation to change in alveolar PCO2 (delta VI/delta PACO2), compared with saline control. Breathing pattern at mean CO2-stimulated ventilation of 25 l/min showed significantly decreased respiratory frequency, increased tidal volume, and prolonged inspiratory time compared with saline. Resting breathing pattern also showed significantly increased tidal volume and inspiratory time. In nine of the same subjects gargling a lidocaine solution adequate to extinguish gag response without altering cough threshold did not change delta VI/delta PACO2 or ventilatory pattern during CO2-stimulated or resting ventilation compared with saline. These results suggest that lower but not upper oropharyngeal vagal airway receptors modulate breathing pattern during hypercapnic as well as resting ventilation but do not affect delta VI/delta PACO2.


1985 ◽  
Vol 58 (6) ◽  
pp. 1988-1996 ◽  
Author(s):  
M. Saetta ◽  
J. P. Mortola

We have studied the breathing pattern (minute ventilation VE, tidal volume VT, and respiratory rate f) in newborn rats before and during barbiturate (20–30 mg/kg ip) or ketamine anesthesia (40–80 mg/kg ip). Animals were intact and prone in a flow plethysmograph in thermoneutral conditions. Before anesthesia, CO2 breathing (5 min in 5% and 5 min in 10% CO2 in O2) resulted in a substantial increase in VE (169 and 208%, respectively), which was maintained throughout the entire CO2 breathing period. This indicates that, despite the extremely large VE per kilogram at rest, in these small animals there is still a large reserve for a sustained increase in VE. During barbiturate, the resting VE dropped to 45% of control, due to a reduction in VT (83%) and f (59%). This latter result was due to a prolongation of the expiratory time (214%) with no significant changes in inspiratory time. CO2 response was also much depressed, to approximately 63% of the control. The late portion of the expiratory flow-volume curves, the slope of which represents the expiratory time constant of the system, was similar before and during anesthesia in approximately 50% of the animals, whereas it increased during anesthesia in the remaining animals. Although compliance of the respiratory system was generally unaltered, the increased impedance during anesthesia probably reflected an increased resistance. Qualitatively similar results were obtained during ketamine anesthesia. Therefore, as observed in adult mammals, anesthesia in newborn rats has a marked depressant effect on resting breathing pattern and CO2 response, occasionally accompanied by an increase in the expiratory impedance of the respiratory system.


1980 ◽  
Vol 48 (4) ◽  
pp. 577-580 ◽  
Author(s):  
J. Askanazi ◽  
P. A. Silverberg ◽  
R. J. Foster ◽  
A. I. Hyman ◽  
J. Milic-Emili ◽  
...  

The effects of ventilatory apparatus on breathing pattern and gas exchange were studied in normal supine subjects. Using a canopy system, measurements of O2 consumption, CO2 production, tidal volume (VT), frequency (f), minute ventilation, mean inspiratory flow, and inspiratory, and expiratory time (TI and TE) were made and compared to data obtained with the use of a mask (m) and mouthpiece plus noseclip (mp + nc). Use of the m or mp + nc caused a 32.5 and 15.5% increase in VT, respectively, whereas f, TI, and TE remained unchanged. As TI did not change the increase in VT was caused entirely by increased inspiratory flow.


1979 ◽  
Vol 47 (1) ◽  
pp. 192-196 ◽  
Author(s):  
J. Askanazi ◽  
J. Milic-Emili ◽  
J. R. Broell ◽  
A. I. Hyman ◽  
J. M. Kinney

Ventilatory patterns during rest, CO2 inhalation (2, 3, and 4%) and three levels of exercise were analyzed in supine men using a canopy system for noninvasive measurements. Changes in tidal volume (VT) and breathing frequency (f) with equal increases in minute ventilation (VE) differed significantly during exercise and CO2 inhalation. Increases in VE during exercise was accompanied by increases in VT and f. During CO2 inhalation, the change in frequency was less than during exercise. However, when analyzed in terms of inspiratory flow (VT/TI) and inspiratory duty cycle (TI/Ttot), the response to both stimuli was similar. With increases to twice control VE both TI/Ttot and VT/VI increased. Thereafter only VTTI increased with increasing VE. At rest, inspiratory time on a breath by breath basis increased minimally with VT, while changes in inspiratory flow accounted for the variability in VT. These two respiratory stimulants appear to increase ventilation through different mechanisms when analyzed in terms of VT and f. However, changes in inspiratory flow and duty cycle are similar in both.


PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 652-655
Author(s):  
Jonathan M. Couriel ◽  
Anthony Olinsky

The ventilatory response to acute hypercapnia was studied in 68 parents of victims of sudden infant death syndrome and 56 control subjects. Tidal volume, inspiratory time, and total respiratory cycle time were measured before and immediately after a vital capacity breath of 13% CO2 in oxygen. Instantaneous minute ventilation, mean inspiratory flow (tidal volume/inspiratory time), and respiratory timing (inspiratory time/total respiratory cycle time) were calculated. Both groups of subjects showed a marked increase in tidal volume (48.4% ± 26.5%), instantaneous minute ventilation (56% ± 35%), and tidal volume/inspiratory time (56.8% ± 33.5%) after inhalation of the test gas, with little change in inspiratory time/total respiratory cycle time. There were no significant differences between the two groups for ventilation before or after inhalation of the test gas. The ventilatory response to acute hypercapnia is mediated by the peripheral chemoreceptors. These results suggest that an inherited abnormality of peripheral chemoreceptor function is unlikely to be a factor leading to sudden infant death syndrome.


1984 ◽  
Vol 57 (2) ◽  
pp. 475-480 ◽  
Author(s):  
C. Weissman ◽  
J. Askanazi ◽  
J. Milic-Emili ◽  
J. M. Kinney

A mouthpiece plus noseclip (MP & NC) is frequently used in performing measurements of breathing patterns. Although the effects the apparatus exerts on breathing patterns have been studied, the mechanism of the changes it causes remains unclear. The current study examines the effects on respiratory patterns of a standard (17-mm-diam) MP & NC during room air (RA) breathing and the administration of 2 and 4% CO2 in normal volunteers and in patients 2–4 days after abdominal operation. When compared with values obtained with a noninvasive canopy system, the MP & NC induced increases in minute ventilation (VE), tidal volume (VT), and mean inspiratory flow (VT/TI), but not frequency (f) or inspiratory duty cycle, during both RA and CO2 administration. The percentage increase in VE, VT, and VT/TI caused by the MP & NC decreased as the concentration of CO2 increased. During RA breathing, the application of noseclip alone resulted in a decrease in f and an increase in VT, but VE and VT/TI were unchanged. The changes were attenuated during the administration of 2 and 4% CO2. Reducing the diameter of the mouthpiece to 9 mm abolished the alterations in breathing pattern observed with the larger (17-mm) diameter MP.


1994 ◽  
Vol 77 (6) ◽  
pp. 2703-2708 ◽  
Author(s):  
H. Burnet ◽  
M. Bascou-Bussac ◽  
C. Martin ◽  
Y. Jammes

In mechanically ventilated patients the natural gas-conditioning process of the upper airways is bypassed by the use of an endotracheal tube or a tracheostomy. We hypothesized that under these conditions the breathing pattern may greatly influence the convective respiratory heat loss (Cr). Cr values were computed from minute ventilation (VE) and inspiratory and expiratory gas temperatures, which were measured in six patients under mechanical ventilation for the management of cranial trauma. In each patient the effects of 11–20 different breathing patterns were investigated. Relationships between Cr and VE and between combined tidal volume and respiratory frequency were obtained by simple and multiple linear regression methods, respectively. Comparison of the standard errors of estimate indicated that multiple linear regression gives the best fit. Thus, Cr was highly dependent on the breathing pattern and was not related only to VE. For the same VE value, Cr was higher when VE was achieved with high tidal volume and low respiratory frequency. These data are consistent with previous studies in which thermal exchanges through the upper airways were taxed by hyperventilation of frigid air.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Paulina M. Getsy ◽  
Sripriya Sundararajan ◽  
Walter J. May ◽  
Graham C. von Schill ◽  
Dylan K. McLaughlin ◽  
...  

AbstractThe roles of endothelial nitric oxide synthase (eNOS) in the ventilatory responses during and after a hypercapnic gas challenge (HCC, 5% CO2, 21% O2, 74% N2) were assessed in freely-moving female and male wild-type (WT) C57BL6 mice and eNOS knock-out (eNOS-/-) mice of C57BL6 background using whole body plethysmography. HCC elicited an array of ventilatory responses that were similar in male and female WT mice, such as increases in breathing frequency (with falls in inspiratory and expiratory times), and increases in tidal volume, minute ventilation, peak inspiratory and expiratory flows, and inspiratory and expiratory drives. eNOS-/- male mice had smaller increases in minute ventilation, peak inspiratory flow and inspiratory drive, and smaller decreases in inspiratory time than WT males. Ventilatory responses in female eNOS-/- mice were similar to those in female WT mice. The ventilatory excitatory phase upon return to room-air was similar in both male and female WT mice. However, the post-HCC increases in frequency of breathing (with decreases in inspiratory times), and increases in tidal volume, minute ventilation, inspiratory drive (i.e., tidal volume/inspiratory time) and expiratory drive (i.e., tidal volume/expiratory time), and peak inspiratory and expiratory flows in male eNOS-/- mice were smaller than in male WT mice. In contrast, the post-HCC responses in female eNOS-/- mice were equal to those of the female WT mice. These findings provide the first evidence that the loss of eNOS affects the ventilatory responses during and after HCC in male C57BL6 mice, whereas female C57BL6 mice can compensate for the loss of eNOS, at least in respect to triggering ventilatory responses to HCC.


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